neurodevelopmental etiology Flashcards
in 1980, crow developed:
type 1 and type 2 schizophrenia
focus of type 1 and type 2 schizophrenia:
primarily structural changes after the onset
some brain imaging machines:
CAT or CT scan, PET scan, MRI, fMRI, DTI
the development of what created PET scan?
radioligands
CT scan uses:
X-rays of the head taken from many directions then processed using computer program
MRI uses:
strong magnetic fields, magnetic field gradients, and radio waves to generate complete images of brain
PET scan uses:
radioactive substances known as radio tracers to visualize and measure changes in metabolic processes and in physiological activities
fMRI uses:
MRI techniques by detecting changes associated with blood flow
Diffusion tenor imagine (DTI) uses:
MRI technique that measures diffusion of water in tissue in order to produce neural tract images
early CT studies detect larger:
lateral ventricles possibly suggesting loss of brain matter
early MRI studies detect reductions in:
overall brain size
Later MRI studies demonstrate reductions in/gets worse with:
thickness of the cortex that is present at the onset of illness and gets worse with disease progression
neurodevelopmental hypothesis:
not only is schizophrenia associated with structural pathology, data has also suggested that the pathology is in the form of a structural defect
the brain takes years of fine tuning before the brain functions in the:
same way as an adult and has adult like microstructure
synaptogensis:
neurons start making connections and sends out projections to nearby neurons. synapse formation begins contributing in part of growth of grey matter
grey matter changes in childhood to adolescence:
cortical thickness decreases, synapses rearranged and pruned, greater efficiency
white matter changes in childhood to adolescence:
myelination increases, greater connectivity, greater efficiency
synapse rearrangement steps: (3)
- release and uptake of neurotrophic factors
- neurons receiving insufficient neurotropic factors die
- axonal processes complete for limited neurotropic factor
active synapses likely take up:
neurotrophic factors that maintains the synapse
inactive synapses get too little:
trophic factors to maintain stable
more synapses equals ____ cortex
thicker
pruned synapses equals ____ cortex
thinner
possibility 1 of schizophrenia as a neurdevelopmental disorder:
presence of an early developmental “insult” that is latent throughout development but not does manifest behaviorally until later when brain can no longer compensate
possibility 2 of schizophrenia as a neurdevelopmental disorder:
imbalance in inhibitory and excitatory neural activity isn’t a big deal until adolescence is required for the “fine tuning” of higher cognitive function
table stages of schizophrenia diagnostics:
features, diagnosis, disability, intervention
evidence for disruptions in brain development have been identified at every:
stage of schizophrenia
primary differences in brain of those with schizo and healthy brain (3)
- deficits in myelination (reduced communication)
- earlier decline in prefrontal excitatory synapses ( excessive pruning)
- deficit in the development of inhibitory synapses (reduced interneuron activity)
primary cell types include those that are involved in:
dopamine and glutamate signaling
glutamate responsible for:
learning and memory
dopamine located in ___ parts of brain and glutamate located in ___ part of brain:
midbrain and striatum; cortex
mesocortical pathway responsible for:
cognitive and executive function
negative symptoms are:
HYPOdopaminergic
mesolimbic pathway responsible for:
regulation of emotional behavior
positive symptoms are:
HYPERdopaminergic
tuberinfundibular pathway responsible for:
regulation of prolactin secretion
nigrostriatal pathway responsible for:
motor control
in the shchizo brain, dopamine levels in the mesolimbic pathway are:
increase causing positive symptoms of schizo. high levels
dopamine levels in the mesocortical pathway are:
decreased, leading to negative and cognitive symptoms. low levels
the predominant “go” neurotransmitter in the brain is:
glutamate
evidence implicating glutamate hypothesis: (3)
- post mortem changes in NMDA receptors
- NMDA-recoptor antagonists can cause psychotic symptoms
- some glutamatergic drugs have shown promise in treated schizo
steps in glutamatrgic and dopaminergic pathways: (4)
- reduced NMDA receptor availability/ functioning on GABAergic interneurons
- disinhibition of glutamatrgic projections onto midbrain dopamine neurones
- increase glutamate release
- increase activation of dopaminergic neurones
most glutamtergic excitatory synapses occur one small protrusions along dendrites called:
dendritic spines
during development and adulthood, changes in dendritic spine number and shape accompany:
synapse formation, cell maintenance, and cell elimination allowing remodeling of connectivity within neuronal circuits
